Nitroxidergic innervation of human cerebral arteries

Taktakishvili, Otar; Lin, Leou-Chyr; Vanderheyden, Andrew D.; Nashelsky, Marcus; Talman, William T.

doi:10.1016/j.autneu.2010.04.012

Cited by 7 publications

(7 citation statements)

References 14 publications

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“…The large arteries at the base of the brain in all species, including human, receive dense sympathetic and parasympathetic innervations (3,6,8,31,45). The functional role of these innervations in controlling regional cerebral circulation, however, remains debatable due to inconsistent results obtained in animal studies (4,16,34,35,36).…”

Section: Discussionmentioning

confidence: 99%

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Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats

Chang

Lee

Chen

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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The close apposition between sympathetic and parasympathetic nerve terminals in the adventitia of cerebral arteries provides morphological evidence that sympathetic nerve activation causes parasympathetic nitrergic vasodilation via a sympathetic-parasympathetic interaction mechanism. The decreased parasympathetic nerve terminals in basilar arteries (BA) of spontaneously hypertensive rat (SHR) and renovascular hypertensive rats (RHR) compared with Wistar-Kyoto rats (WKY), therefore, would diminish this axo-axonal interaction-mediated neurogenic vasodilation in hypertension. Increased basilar arterial blood flow (BABF) via axo-axonal interaction during sympathetic activation was, therefore, examined in anesthetized rats by laser-Doppler flowmetry. Electrical stimulation (ES) of sympathetic nerves originating in superior cervical ganglion (SCG) and topical nicotine (10-30 μM) onto BA of WKY significantly increased BABF. Both increases were inhibited by tetrodotoxin, 7-nitroindazole (neuronal nitric oxide synthase inhibitor), and ICI-118,551 (β(2)-adrenoceptor antagonist), but not by atenolol (β(1)-adrenoceptor antagonist). Topical norepinephrine onto BA also increased BABF, which was abolished by atenolol combined with 7-nitroindazole or ICI-118,551. Similar results were found in prehypertensive SHR. However, in adult SHR and RHR, ES of sympathetic nerves or topical nicotine caused minimum or no increase of BABF. It is concluded that excitation of sympathetic nerves to BA in WKY causes parasympathetic nitrergic vasodilation with increased BABF. This finding indicates an endowed functional neurogenic mechanism for increasing the BABF or brain stem blood flow in coping with increased local sympathetic activities in acutely stressful situations such as the "fight-or-flight response." This increased blood flow in defensive mechanism diminishes in genetic and nongenetic hypertensive rats due most likely to decreased parasympathetic nitrergic nerve terminals.

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Section: Discussionmentioning

confidence: 99%

“…Human basilar arteries also receive sympathetic (3,21) and nitrergic neurons (45,50), which are functional in regulating the cerebral circulation (2,38,46). Reports by many indicate that cigarette smoking frequently increases cerebral blood flow (5,24).…”

Section: Discussionmentioning

confidence: 99%

Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats

Chang

Lee

Chen

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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“…In these neurons, NO is frequently coexpressed with VIP, and the relative importance of NO and VIP in mediating smooth muscle relaxation varies with the target tissue. For example, the sphenopalatine ganglion provides nitroxidergic vasodilator innervation of facial and cerebral blood vessels 47 and pelvic ganglia trigger NO-mediated vasodilation of erectile tissue. A significant proportion of myenteric motor neurons and interneurons, particularly those in the colon and rectum, express nNOS; this suggests NO is important for maintenance of normal colon motility, colonic reflexes, and defecation.…”

Section: Protein Quality Controlmentioning

confidence: 99%

Nitric oxide

Benarroch

2011

Neurology

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Nitric oxide (NO) is a gaseous chemical transmitter that is produced from the amino acid L-arginine by the members of the NO synthase (NOS) family of proteins. NO is involved in several important functions in the CNS and peripheral nervous system (PNS), including modulation of neurotransmission and regulation of local blood flow and immune responses. NO interacts with intracellular targets to trigger several signal transduction pathways. In the CNS, NO participates in synaptic modulation and plasticity, control of sleep, body temperature, and neurosecretion. In the PNS, NO mediates vasodilation and relaxation of the visceral smooth muscle. However, when produced in excess and in the setting of oxidative stress, NO becomes toxic, leading to formation of reactive nitrogen species (RNS), which cause cellular damage. These neurotoxic effects of NO derivatives may be involved in the pathogenesis of cerebral ischemia, inflammation, neoplasia, and neurodegenerative disorders. There are several comprehensive reviews on the physiologic and pathophysiologic roles of NO in the nervous system. 1-12 NITRIC OXIDE SYNTHASES Catalytic activity.The NOS family of enzymes catalyzes the oxidation of L-arginine to form L-citrulline and NO (figure 1). NOS is a dimeric enzyme; each monomer is composed of 2 distinct catalytic domains, an amino (NH2)-terminal oxygenase domain and a carboxy (COOH)-terminal reductase domain. The oxygenase domain is the binding site for heme, oxygen (O 2 ), tetrahydrobiopterin (BH4), and L-arginine; the reductase domain binds flavin adenine dinucleotide (FAD), flavin mononucleotide (FMN), and reduced nicotinamide-adenine dinucleotide phosphate (NADPH). The catalytic mechanism involves flavin-mediated electron transport from NADPH to the heme center, where O 2 is reduced and incorporated into the guanidine nitrogen of L-arginine, producing NO and L-citrulline.

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“…Neuronal nitric oxide synthase (nNOS), the enzyme responsible for neuronal synthesis of NO, is found in nerve fibers that surround and innervate cerebral arteries in experimental animals and in humans (Nozaki et al, 1993; Taktakishvili et al, 2010). NO may modify the function of a wide variety of proteins, including ASICs (Wang et al, 2012), by two major pathways (Ahern et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Acid-sensing ion channel 1 and nitric oxide synthase are in adjacent layers in the wall of rat and human cerebral arteries

Lin

Jin

Nashelsky

et al. 2014

Journal of Chemical Neuroanatomy

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Extracellular acidification activates a family of proteins known as acid-sensing ion channels (ASICs). One ASIC subtype, ASIC type 1 (ASIC1), may play an important role in synaptic plasticity, memory, fear conditioning and ischemic brain injury. ASIC1 is found primarily in neurons, but one report showed its expression in isolated mouse cerebrovascular cells. In this study, we sought to determine if ASIC1 is present in intact rat and human major cerebral arteries. A potential physiological significance of such a finding is suggested by studies showing that nitric oxide (NO), which acts as a powerful vasodilator, may modulate proton-gated currents in cultured cells expressing ASIC1s. Because both constitutive NO synthesizing enzymes, neuronal nitric oxide synthase (nNOS) and endothelial NOS (eNOS), are expressed in cerebral arteries we also studied the anatomical relationship between ASIC1 and nNOS or eNOS in both rat and human cerebral arteries. Western blot analysis demonstrated ASIC1 in cerebral arteries from both species. Immunofluorescent histochemistry and confocal microscopy also showed that ASIC1-immunoreactivity (IR), colocalized with the smooth muscle marker alpha-smooth muscle actin (SMA), was present in the anterior cerebral artery (ACA), middle cerebral artery (MCA), posterior cerebral artery (PCA) and basilar artery (BA) of rat and human. Expression of ASIC1 in cerebral arteries is consistent with a role for ASIC1 in modulating cerebrovascular tone both in rat and human. Potential interactions between smooth muscle ASIC1 and nNOS or eNOS were supported by the presence of nNOS-IR in the neighboring adventitial layer and the presence of nNOS-IR and eNOS-IR in the adjacent endothelial layer of the cerebral arteries.

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Nitroxidergic innervation of human cerebral arteries

Cited by 7 publications

References 14 publications

Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats

Sympathetic activation increases basilar arterial blood flow in normotensive but not hypertensive rats

Nitric oxide

Acid-sensing ion channel 1 and nitric oxide synthase are in adjacent layers in the wall of rat and human cerebral arteries

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